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- How Common Are STDs?
- STD Prevention and Treatment
- Bacterial STDs
- Viral STDs
- Parasitic STDs
- STDs Transmitted by Other Means
- Sequellae of STDs (Possible Complications)
- STDs and HIV
- STDs Increase Risk for HIV
- How HIV Impacts Specific STDs
- Do STD Programs Influence HIV Rates?
- STD-HIV Recommendations
- Resources
- Selected Sources
Sexually transmitted diseases (STDs), formerly known as venereal diseases, are diseases that are spread from person to person through sexual activity. There are over 20 diseases that can be transmitted sexually; they may be caused by bacteria, viruses, or parasites (see below for information on specific STDs). Some conditions, for example vaginal candidiasis and bacterial vaginosis are often not transmitted sexually, but are nevertheless associated with symptoms similar to those of STDs, such as genital inflammation.
Some STDs, such as syphilis and genital herpes, can be characterized by genital ulcers or sores. Others, such as gonorrhea and chlamydia, can cause inflammation of the urethra (urethritis) or cervix (cervicitis) and genital discharge. However, many people with STDs, especially women, do not have any noticeable symptoms. In fact, M.L. Lamb of the U.S. Centers for Disease Control and Prevention (CDC) presented study results at the XIII International AIDS Conference in Durban, South Africa, this past July showing that the majority of STD cases were asymptomatic, or "silent"; rates of asymptomatic STDs (including gonorrhea, syphilis, chlamydia, and trichomoniasis) were nearly 50% in men and well over 50% in women. People can transmit STDs even if they have no symptoms.
Any condition characterized by genital sores and inflammation -- whether sexually transmitted or not -- can promote HIV transmission, both by making a person with an STD more likely to contract HIV, and by increasing the chances that a person coinfected with HIV and an STD will transmit HIV to a sexual partner.
Any sexually active person who experiences pain or burning during urination, genital discharge, sores or a rash in the genital or anal areas, or pain during sexual intercourse should see their health-care provider or visit an STD clinic. Because many people with HIV do not have symptoms, annual screening is recommended for sexually active people.
How Common Are STDs?
STDs are among the most common infectious diseases around the world. The U.S. has the highest STD rates in the industrialized world. The CDC estimates that there are over 15 million new cases of STDs in the U.S. annually (incidence); when the numbers of existing cases of chronic, incurable STDs are factored in, the numbers are much higher (prevalence). Globally, the World Health Organization (WHO) estimated in 1995 that 333 million new cases of curable (i.e., bacterial) STDs occur annually.
In the U.S., the incidence of STDs is highest in teenagers and young adults; people under age 25 account for about two-thirds of new sexually transmitted infections. STD rates are higher in the southeast region of the U.S. and in certain racial/ethnic groups (for example, the syphilis rate among African-Americans is 50 times higher than that among whites). Rates are also high among some populations of young men who have sex with men. STDs are associated with socioeconomic factors such as poverty and lack of regular health care, and with behavioral factors such as number of sex partners. The incidence of some STDs -- such as chlamydia and herpes -- has risen in the U.S. over the past decade, likely due in part to improved surveillance and detection methods. However, other STDs -- such as syphilis -- have become less common.
STD Prevention and Treatment
The same safer sex precautions recommended to prevent HIV transmission -- the use of latex condoms and other barriers -- reduce the risk of transmission of some STDs. However, because STDs can be spread through contact with lesions on the skin, which may occur on areas that are not covered by condoms or barriers, these methods are not completely effective. It is good practice to check sexual partners for sores, discharge, or other symptoms, but because people with no visible symptoms may still transmit STDs, this precaution is not foolproof. Because the risk factors for the various STDs are similar, a person who contracts one STD should be checked for others as well. The CDC recommends that people who are sexually active and not in a mutually monogamous relationship receive regular STD screenings, since early detection and treatment can prevent many of the serious adverse consequences associated with STDs.
Bacterial STDs (e.g., chancroid, chlamydia, gonorrhea, and syphilis) can be treated with antibiotics and are completely curable if detected and treated early. Once treatment begins, a person should take the full course of medication prescribed, even if symptoms disappear. Sexual partners should be treated at the same time to avoid passing an infection back and forth. Viral STDs (e.g., genital herpes, and human papillomavirus) are not curable (although they can be treated), and remain in the body for life. Several of the drugs used to treat STDs should not be used by pregnant women; any woman who is experiencing STD symptoms and may be pregnant should discuss treatment with an experienced health-care provider. See the treatment information below for specific STDs.
Bacterial STDs
Chancroid, caused by the Hemophilus ducreyi bacterium, is an ulcerative STD that causes soft lesions that are usually located on the genitals. The disease is endemic in some areas of the U.S. Chancroid lesions usually begin as elevated bumps that fill with pus and develop into open sores; usually there is only one ulcer, but in some cases there may be more. Men are more likely to have painful lesions than women; chancroid in women is often asymptomatic. The soft, tender chancroid lesions can be distinguished from syphilis chancres, which are typically firm and painless. Symptoms usually appear 3-10 days after exposure to the bacterium. About one-half of people with chancroid also have painful, swollen lymph nodes in the groin, usually on one side; the enlarged glands may fuse into a large mass called a bubo. Some people also experience genital discharge, painful urination or defecation, and pain during intercourse. Diagnosis is done by isolating H. ducreyi from a lesion and ruling out other STDs with similar symptoms such as syphilis and genital herpes.
Chancroid is treated with an antibiotic such as azithromycin, ceftriaxone, ciprofloxacin, or erythromycin. Buboes may need to be surgically drained.
Chlamydia is caused by the Chlamydia trachomatis bacterium. It is one of the most common STDs in the U.S., with an estimated 3-4 million new cases annually; as many as one in 20 women of childbearing age may be infected. Chlamydia is the most common cause of nongonococcal urethritis (NGU). Its symptoms are similar to those of gonorrhea, and can include pain or burning during urination (especially in the morning); inflammation of the urethra, cervix, or rectum; pain and itching of the penis, vagina, or anus; and a whitish discharge from the penis or vagina. Symptoms typically begin two to three weeks after exposure to the bacterium. However, chlamydia is asymptomatic in as many as two-thirds of cases, especially in women, and regular screening is therefore recommended for sexually active women. One strain of chlamydia, prevalent in tropical climates but rare in the U.S., causes an STD called lymphogranuloma venereum (LGV) that is characterized by swollen lymph nodes in the groin.
Chlamydia is diagnosed by a culture test of genital fluid, a DNA amplification assay, or a recently approved urine test. It can be treated with antibiotics including azithromycin (Zithromax), ceftriaxone (Rocephin), doxycycline (Vibramycin), ofloxacin (Floxin), or erythromycin (Ilosone); penicillin is not effective. Because gonorrhea and chlamydia commonly occur together, combination antibiotic treatment is often given to combat both infections. If chlamydia is left untreated, it can cause pelvic inflammatory disease (PID) in women and epididymitis in men (see below). Chlamydia can be transmitted to newborns during birth, causing conjunctivitis (eye infection) or pneumonia.
Gonorrhea is caused by the Neisseria gonorrhoeae bacterium, which multiplies in warm, moist areas of the body. According to the CDC, U.S. gonorrhea rates increased by 9% in 1998 to 132.9 cases per 100,000 people, after declining for 12 years. Gonorrhea may be transmitted by vaginal, anal, or oral sex, and may affect the urethra, vagina, cervix, rectum, pharynx (throat), or eyes. Symptoms, which typically appear 2-14 days after exposure, include pain or burning during urination or defecation; a yellowish or greenish (pus-like) penile, vaginal, cervical, or rectal discharge; swelling and tenderness of the vulva; sore throat; and a false urge to urinate or defecate. An estimated 10% of men and up to 80% of women have no symptoms.
Gonorrhea is diagnosed using a Gram stain, in which a sample of genital fluid is dyed and examined under a microscope, or a DNA test; a urine test for gonorrhea is also available. In the 1980s, Neisseria gonorrhoeae developed resistance to penicillin and tetracycline (Sumycin, Achromycin), and the disease is now usually treated with oral antibiotics such as ceftriax-one, cefixime (Suprax), ciprofloxacin (Cipro), ofloxacin, azithromycin, or by injection. However, the incidence of fluoroquinolone and macrolide antibiotic resistant gonorrhea is rising; in September the CDC announced the first reported cases of azithromycin-resistant Neisseria gonorrhoeae in the U.S. Untreated gonorrhea can lead to PID or epididymitis, as well as damage to the joints. In pregnant women, gonorrhea is associated with premature labor, miscarriage, and stillbirth, and it may be transmitted to an infant during birth.
Granuloma Inguinale
Granuloma inguinale, also known as donovanosis, is caused by the Calymmatobacterium granulomatis bacterium. The disease is rare in the U.S. but endemic in some tropical areas of the world. Granuloma inguinale is characterized by painless, red, "beefy" lesions not accompanied by swollen groin lymph nodes. The disease is diagnosed by the identification of so-called Donovan bodies in a biopsy sample. Granuloma inguinale is treated with a course of antibiotics such as TMP-SMX (Bactrim, Septra), doxycycline, ciprofloxacin, or erythromycin. Pregnant and lactating women should be treated with erythromycin. In some cases, relapse can occur 6-18 months after effective initial therapy.
Syphilis, caused by the Treponema pallidum bacterium, has been called "the great imitator" because its symptoms vary widely and can mimic those of many other diseases. Syphilis is becoming rarer in the U.S.; in 1998, rates were the lowest ever seen since tracking began in 1941, at an average of 2.6 cases per 100,000 people (although the rate varies considerably by region and ethnic group). In 1999, the CDC launched a campaign to eradicate the disease in this country within five years.
Syphilis has a complex pathogenesis (course of development) characterized by primary, secondary, latent, and tertiary stages. Primary syphilis typically begins with a single sore or ulceration called a "chancre" on the penis or vulva, which appears 10-90 days after exposure to the bacterium; the chancre may also develop on the cervix, lips, or tongue, inside the vagina or anus, or on other parts of the body. The firm, usually painless lesion typically resolves without treatment after 1-6 weeks. Some people with primary syphilis have no symptoms. Secondary syphilis is characterized by flu-like symptoms including fatigue, sore throat, headache, joint aches, loss of appetite, and swollen glands; some people also experience patchy hair loss. People with this stage of disease may also develop a rash, which may range from round, brownish blotches (described as looking like pennies) to a red or pustular appearance; the rash may appear anywhere on the body, and usually affects the palms of the hands and soles of the feet. Secondary symptoms may last for a few weeks to a few months, and may come and go over the course of 1-2 years.
If syphilis remains untreated, symptoms disappear and the person can no longer transmit the disease sexually, but the bacteria remain latent (inactive) for years or even decades. Symptomatic late-stage or tertiary syphilis involves damage to the eyes, heart, bones, joints, and nervous system, and may be fatal. Some people develop soft tissue tumors called gummas. Syphilis that affects the brain is known as neurosyphilis, and may be characterized by headaches, seizures, personality changes, or dementia. A pregnant woman can transmit syphilis to her child, leading to stillbirth or to serious physical and mental disabilities in the newborn, a condition known as congenital syphilis.
Syphilis is diagnosed using the rapid plasma reagin (RPR) or Venereal Disease Research Laboratories (VDRL) blood tests, and confirmed with fluorescent treponemal antibody absorption (FTA-ABS) or Treponema pallidum hemagglutination antibody (TPHA) tests; darkfield microscope examination (which looks at an object illuminated from the side against a dark background) may also be used. Early-stage syphilis can be treated with a single injection of benzathine penicillin; more advanced stages may require longer courses of treatment. Ceftriaxone, doxycycline, tetracycline, or erythromycin may be used if a person is allergic to penicillin, although in some cases penicillin desensitization is recommended. Although syphilis antibodies remain in the body for life, a person can be reinfected with syphilis.
Viral STDs
Genital Herpes
Genital herpes is caused by the herpes simplex virus (HSV). Although HSV type 2 is classically associated with genital lesions and HSV type 1 is associated with oral lesions ("cold sores"), either type can affect either area of the body. HSV-2 is very common, with an estimated 45-60 million people infected in the U.S. and 1 million new infections annually; as many as 20% of U.S. adults may be infected with HSV type 2. Herpes is characterized by blisters on the genitals, inside the vagina or rectum, or around the mouth. Sores typically develop 2-20 days after exposure to the virus, but may develop years later. The blisters often break open, forming painful ulcers. Some people also experience fever and swollen glands. The sores usually dry up, scab over, and heal without scarring after 2-7 weeks. Some people infected with HSV never develop recognizable symptoms. Studies have shown that HSV is present in genital fluids of people with genital herpes, even when they do not have active herpes lesions. Even after genital herpes lesions heal, the virus is not eradicated; instead it takes up residence in nerve endings and may be reactivated periodically.
Recurrent outbreaks are associated with several factors including emotional stress, illness, exposure to ultraviolet light, menstruation, and a weakened immune system. Recurrences may be preceded by prodromal (precursor) symptoms including itching and tingling in the area in which the outbreak will occur, pain in the groin or buttocks, and sometimes malaise. Transmission may occur during an active outbreak, but some people can transmit the virus when they have no symptoms, a phenomenon known as asymptomatic shedding, which may be due to the presence of HSV in genital fluids. Recurrent outbreaks are typically milder than the initial episode, and outbreak frequency often decreases over time. Herpes can be transmitted from a mother to her newborn -- especially if she is experiencing her first episode -- leading to premature delivery, miscarriage, eye and nerve damage, mental retardation, and possibly death.
HSV infection is diagnosed with a blood test to detect antibodies. Although there is no cure for herpes, nucleoside analog antiviral drugs -- acyclovir (Zovirax), valacyclovir (Valtrex), famciclovir (Famvir), and topical penciclovir (Denavir) -- can suppress the virus and reduce the frequency, length, and severity of outbreaks, as well as the risk of transmitting herpes. Immediate treatment of infants born with herpes decreases the chance that they will develop serious illness. At the 40th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) this past September, Spotswood Spruance, PharmD, and colleagues reported on a study of a new vaccine for genital herpes. The Simplirix vaccine, made by SmithKline Beecham, reduced the incidence of HSV type 2 infection by about 75% in HSV-negative women whose partners already were infected with herpes. However, the vaccine had "absolutely no effect" on HSV type 2 incidence in "high-risk" men, according to Spruance.
Human Papillomavirus and Genital Warts
Human papillomavirus (HPV) is a family of over 60 strains of virus that are associated with warts. Various so-called "low-risk" strains are associated with common warts or genital warts (also called condyloma accuminata). "High-risk" strains are associated with cervical, anal, or penile dysplasia (abnormal precancerous cell growth) and cancer. Many people are coinfected with both high-risk and low-risk strains. HPV is one of the most common STDs. It is estimated that 5.5 million new HPV infections occur in the U.S. annually, with a cumulative total of 30-40 million cases. The virus is spread by direct skin-to-skin contact with an infected person, and may occur even if the person is asymptomatic.
Genital warts usually appear a few weeks to several months after exposure. They typically begin as tiny bumps -- which are usually not painful or itchy -- on the penis, scrotum, vulva, or anus; inside the vagina or rectum; or on the cervix. The warts often occur in clusters and, if untreated, many grow into large fleshy masses; growth is more rapid in pregnant woman and in people with compromised immune systems. However, many people with HPV infection have no visible symptoms.
The presence of HPV can be detected by a blood test. Warts can be detected by visual inspection; application of vinegar may help make small warts more visible. There is no cure for HPV, and the virus remains in the body for life. However, there are a number of treatments for warts and dysplasia. Warts may be removed by freezing with liquid nitrogen (cryosurgery), burning (electrocauterization), or conventional surgery. Topical remedies include podofilox (Condylox), podophyllin (Podofin), trichloroacetic acid, 5-fluorouracil, and imiquimod (Aldara); podofilox, podophyllin, and 5-fluorouracil should not be used in pregnant women. Because many people report that podophyllin treatment is painful, more rapid methods of removing warts are preferred. If warts do not respond to these treatments, a doctor may inject interferon-alpha directly into the wart.
Dysplasia, which can progress to cancer, is quite treatable in early stages. The progressive stages of dysplasia are known by various names including cervical or anal intracellular neoplasia (CIN and AIN, respectively) and squamous intraepithelial lesions (SIL). Pap smears, which involve looking at a sample of cells under a microscope, are used to detect the condition as it develops. Regular cervical Pap smears have significantly reduced the death rate from cervical cancer, and some experts now recommend anal Pap smears for certain populations, including people who engage in receptive anal intercourse. An instrument called a colposcope also may be used to view cervical or anal cell changes. Early-stage dysplasia may be treated by freezing, burning, or cutting away the top layers of tissue, in the hope that normal cells will grow in its place. A promising HPV vaccine is currently under development by Merck Laboratories. (For more information on CIN, see BETA, June 1996; for more information on HPV and AIN, see BETA, September 1997.)
Parasitic STDs
Pubic Lice
Pubic lice, often referred to as "crabs," are caused by tiny insects called Phthirus pubis or Pediculosis pubis. The insects can spread through close skin-to-skin contact, but also via shared towels, clothing, or bedding. Pubic lice typically live in the pubic hair, but may also take up residence in underarm hair, facial hair, eyebrows, or eyelashes. The primary symptom is itching, which usually begins within five days after exposure; the itching is due to an allergic reaction to the insect bites. Diagnosis is made by detecting the grayish or rust-colored parasites or their white eggs. Pubic lice are treated with over-the-counter topical preparations such as 1% permethrin (Nix) or prescription-strength 5% permethrin (Elimite). The prescription drug lindane (Kwell, Isotox) may also be used, but its use is becoming less common due to widespread resistance. Other options are the new prescription medication methialine (Ovide) and a single 200 mg/kg dose of oral ivermectin (Stromectol). In addition, clothes and bedding should be washed in hot water and disinfected, and lice eggs can be combed out of the hair with a special, fine-toothed comb. Sometimes a second round of treatment is indicated 7-10 days later if a new set of eggs hatches. Sex partners should be evaluated and, if necessary, treated. Hydrocortisone or other over-the-counter anti-itch creams may be used to relieve symptoms during treatment.
Scabies is caused by a mite, Sarcoptes scabiei, that burrows under the skin. The mites are easily transmitted through skin-to-skin contact or by sharing towels, bedding, and clothing. Although scabies can occur on any part of the body, it prefers moist folds, and most often attacks the genital area or the webbing between the fingers and toes. The female mites lay eggs under the skin, usually within ten days of exposure. The primary symptom, which develops within about a month after exposure, is intense itching due to an allergic reaction to the insects' bites; the itching is often worse at night. Some people develop an eczema-like rash. Diagnosis is made by detecting the mites, via a microscopic examination of skin scrapings, or their burrows. The burrows often appear as zigzag lines on the skin, and may be made more visible by applying ink. Treatments include lindane or 5% permethrin cream, which is applied over the entire body from the neck down and left on for 8-10 days; a repeat application may be necessary. Lindane is a highly toxic medication; pregnant or lactating women and children under the age of two should not use lindane. Ivermectin may also be used to treat scabies. Clothes, towels, and bedding should be washed in hot water.
Trichomoniasis is caused by a protozoan parasite called Trichomonas vaginalis. There are an estimated five million new cases of trichomoniasis annually in the U.S. The parasite causes inflammation of the vagina and urethra. Symptoms of trichomoniasis usually appear 3-28 days after exposure to the parasite. The primary symptom in women is a foamy, yellow-green vaginal discharge with a strong "fishy" odor; women may also experience genital irritation or itching, and swelling and redness of the vulva. Although most men with trichomoniasis are asymptomatic, some may experience irritation inside the urethra or under the foreskin, or mild penile discharge. Both women and men may feel a frequent urge to urinate and experience pain or burning during urination. Trichomoniasis in pregnant women can cause premature rupture of placental membranes, leading to pre-term labor; newborns can contract the infection during delivery. Diagnosis is done with a laboratory test of a sample of discharged fluid; the parasite is harder to detect in men. The disease may be treated with a single oral dose of the antiparasitic drug metronidazole (Flagyl). Once they are cured, people may contract trichomoniasis again.
STDs Transmitted by Other Means
Bacterial Vaginosis
Bacterial vaginosis (BV), previously known as nonspecific vaginitis, is the most common cause of vaginal inflammation in women of childbearing age. BV occurs when the dominant bacterial flora of the vagina -- primarily Lactobacillus -- is disturbed, allowing the overgrowth of other bacteria such as Gardnerella vaginalis, Bacteroides, Mobiluncus, Mycoplasma hominis, and Ureaplasma urealyticum. BV is not necessarily transmitted sexually; it is associated with sex with a new partner, douching, use of an intrauterine device for contraception, and changes in vaginal pH. Symptoms of BV include a watery or foamy, grayish or whitish vaginal discharge; abnormal "fishy" odor; pain or itching of the vulva; and burning during urination. Many women with BV are asymptomatic. Pregnant women with BV have higher rates of miscarriages and premature or underweight infants. In some cases, the bacteria that cause BV can make their way to the upper reproductive organs, leading to PID. Diagnosis of BV is done by examining a sample of discharged fluid under a microscope to look for "clue cells." BV may be treated with topical or oral therapies such as metronidazole or clindamycin (Cleocin). BV may recur after initial treatment.
Candidiasis, commonly known as a "yeast infection," is an overgrowth of the Candida albicans fungus, or occasionally other Candida species. Candida albicans occurs normally in the vagina. Candidiasis may affect the entire body and is usually not transmitted sexually, but Candida overgrowth of the vulva and vagina may be spread through sexual activity. Symptoms of vulvovaginal candidiasis include a thick, white, lumpy discharge with a yeasty odor. Women may also experience pain, itching, redness, and swelling of the vulva, as well as pain during urination or sexual intercourse. Women with compromised immune systems may have longer-lasting and more frequent episodes. Candida may also cause an infection of the glans of the penis (balanitis) in men, although this is uncommon.
Candidiasis is diagnosed using a KOH preparation. Many women harbor Candida in the vagina with no symptoms. Unlike BV, candidiasis usually occurs with a normal vaginal pH. Candidiasis is treated with topical or intravaginal antifungal preparations such as clotrimazole (Mycelex, GyneLotrimin), miconazole (Monistat), terconazole (Terazole), or nystatin (Mycostatin); oral fluconazole (Diflucan), itra-conazole (Sporanox), or ketoconazole (Nizoral) may also be used, especially in treatment-resistant or recurrent cases. Candidiasis is common in pregnant women, who should receive only topical, not systemic, treatment. (For more information on candidiasis, see BETA, September 1995, page 28, and June 1995, p. 10.)
Cytomegalovirus (CMV), a member of the herpesvirus family, is best known as an opportunistic infection (OI) that affects people with compromised immune systems, for example due to HIV or immunosupressive drugs used with organ transplants. CMV infection is very common in the general population in the U.S., and a majority of adults harbors the virus. It is present in semen, vaginal fluid, saliva, and urine, and is easily transmitted sexually. CMV is also commonly transmitted from a pregnant woman to her child before birth or through breast-feeding. CMV usually does not cause symptoms in people with healthy immune systems, but some people experience a flu-like or mononucleosis-like illness characterized by fever, fatigue, weakness, and swollen glands. In contrast, immuno-compromised people may develop serious illnesses such as retinitis (an inflammation of the retina of the eye, potentially leading to blindness), colitis (inflammation of the large intestine), polyneuritis (nerve inflammation), or pneumonia. CMV is diagnosed by a blood test or a culture test of body fluids. There is no cure for the disease, and people are thought to carry the virus for life. Disease progression in immuno-compromised persons can be reduced with intravenous antiviral medications such as ganciclovir (Cytovene), foscarnet (Foscavir), or cidofovir (Vistide). HIV-related CMV retinitis may be treated with eye injections or implants. Oral valganciclovir is also effective for HIV-related CMV retinitis. (For more information on CMV, see BETA, December 1994, p. 6.)
Although not primarily appreciated as STDs, some hepatitis viruses can be transmitted through sexual activity. Hepatitis in general refers to an inflammation of the liver. Hepatitis A, caused by the hepatitis A virus (HAV), is spread through the fecal-oral route. It is most often contracted through contaminated food or water, but may also be transmitted through oral-anal sex (rimming) or activities that spread fecal matter to the mouth via the hands, penis, or sex toys. Hepatitis B and C, caused by the hepatitis B virus (HBV) and hepatitis C virus (HCV), respectively, are most often transmitted through blood (e.g., a needlestick injury, sharing of drug injection equipment), but may be transmitted sexually. Both viruses have been detected in the semen and vaginal fluids of infected persons. Sexual transmission is more common with HBV; the CDC estimates that there are about 77,000 sexually transmitted cases of HBV in the U.S. annually. According to CDC estimates, up to 20% of HCV infections may be attributable to sexual contact, but most studies show a much lower rate. An analysis of several different studies revealed an average sexual transmission rate of 1.5% among long-term, monogamous heterosexual partners and up to 10% among long-term, monogamous gay male couples.
Symptoms of hepatitis include nausea, vomiting, fatigue, fever, abdominal pain, and loss of appetite; some people develop jaundice (yellowing of the skin and whites of the eyes). Many people infected with hepatitis B or C have no symptoms. Pregnant women can transmit hepatitis B or C to their infants. Hepatitis is diagnosed using a blood test. Hepatitis A usually resolves without treatment and does not become chronic; a person who has had HAV cannot become infected again. Both HBV and HCV may become chronic, potentially leading to liver scarring (cirrhosis), liver cancer, and liver failure. Chronic carriers of HBV or HCV, whether symptomatic and asymptomatic, can transmit the virus.
HBV and HCV are not easily treated, although there are several FDA-approved drugs. The most common treatments for HBV are interferon-alpha and 3TC (Epivir), and the standard treatment for HCV is interferon-alpha plus ribavirin (Rebetron). HAV and HBV can both be prevented with a vaccine, and vaccination is recommended for sexually active people. (For more information on hepatitis in general, see BETA, January 1998; for more information on HCV, see BETA, Year-End 1999.)
Intestinal Parasites and Bacteria
Several intestinal parasites and bacteria can be spread through sexual activity, especially oral-anal sex or other activities that spread fecal matter to the mouth via the hands, penis, or sex toys. However, worldwide these organisms are most commonly contracted through contaminated food or water. Parasitic organisms in this category include Entamoeba histolytica, Giardia lamblia, and species of Cryptosporidium, Microsporidium, and Isospora. Bacteria that may be transmitted sexually include Salmonella, Shigella, and Escherichia coli. These microbes usually cause gastrointestinal illness (gastroenteritis) characterized by diarrhea, nausea, vomiting, abdominal cramps, fever, and blood in the stools; symptoms typically begin within 36 hours after exposure. Diagnosis is made by examining a fecal sample for specific organisms. Specific parasitic infections are treated with different medications; metronidazole is used for some of the most common organisms. Bacterial infections may be treated with drugs such as ciprofloxacin.
Molluscum Contagiosum
Molluscum contagiosum is a skin infection caused by a virus of the same name. It is transmissible by skin-to-skin contact and by sharing towels, clothing, or razors. The primary symptom is small flesh-colored, gray, or pinkish lesions with a central depression. Lesions may appear anywhere on the body, but are most often seen on the face, torso, thighs, buttocks, groin, or genitals; they may be tender or itchy. They usually appear 2-12 weeks after exposure to the virus and can last two weeks to several years if not removed. Outbreaks may be more extensive and last longer in people with compromised immune systems. Molluscum is diagnosed by the characteristic "umbilicated" appearance of the lesions, or by a microscopic examination of a sample scraped from a lesion. Lesions may be removed surgically or by freezing with liquid nitrogen, and may be treated topically with agents such as podophyllin, cantharidin (Cantharone), phenol, silver nitrate, trichloracetic acid, or iodine.
Sequellae of STDs (Possible Complications)
Pelvic Inflammatory Disease and Epididymitis
Pelvic inflammatory disease (PID) and epididymitis are not STDs, but rather long-term, serious complications of infection with various sexually transmitted organisms. PID is an infection of the upper female reproductive tract including the uterus, ovaries, and fallopian tubes. It is most often caused by Chlamydia trachomatis or Neisseria gonorrhoeae, but is also associated with Bacteriodes species. Bacteria may more easily enter the uterus and fallopian tubes during menstruation; douching may also help bacteria gain access to the internal reproductive organs, and therefore is not recommended. There are an estimated 1 million new cases of PID annually in the U.S.
PID may be asymptomatic at early stages, or may be characterized by symptoms such as vaginal discharge, prolonged menstrual periods, bleeding between periods, abdominal or lower back pain, fever or chills, nausea, painful sexual intercourse, and tenderness during a pelvic examination. The infection may damage the reproductive organs, potentially leading to life-threatening ectopic or tubal pregnany (in which a fertilized egg develops in a fallopian tube rather than the uterus) or infertility.
PID can be diagnosed by a pelvic examination or laparoscopy, in which a small, lighted instrument is inserted into an incision in the abdomen to view the internal organs. PID is treated with antibiotics to control the causative organism(s). Treatment is more successful the earlier it is begun; often the responsible agent cannot be easily identified, so a combination antibiotic regimen is used. In some cases, surgery may be required to remove scar tissue, abcesses, or heavily damaged organs. An estimated one-third of women who have had PID will develop the condition again, and the risk of infertility is increased with each subsequent episode.
Epididymitis is an infection of the epididymis, the tubes that store and carry sperm. As with PID, the causative organism is most often gonorrhea or chlamydia. Symptoms include pain in the testes, scrotum, or abdomen. Untreated infection can progress to infection of the entire testicle (orchitis). Epididymitis, like PID, is treated with antibiotic regimens. In severe cases, surgical removal of the testicle(s) may be necessary.
STDs and HIV
STDs are associated in several ways with HIV. Because STDs and HIV are spread by similar types of sexual activity, people who engage in behaviors that transmit HIV are also more likely to contract STDs, and vice versa. Persons who contract an STD may also have put themselves at risk for HIV and should be tested. Likewise, a person who contracts HIV should be tested for other STDs.
Epidemiological evidence shows that populations and geographical regions in the U.S. with the highest STD rates also tend to have the highest rates of HIV. According to the CDC, "The geographic distribution of heterosexual HIV transmission closely parallels that of other STDs." In the past decade, high HIV incidence rates have shifted toward women infected through heterosexual activity, young adults, African-Americans, and people living in the southeastern U.S., all populations with disproportionately high rates of STDs. At the Durban AIDS conference, J. Hanson and colleagues presented a study of HIV/STD incidence using a mathematical model based on medical records of 10,879 people attending a New Orleans STD clinic. The results suggested that the presence of an ulcerative or non-ulcerative STD increased the risk of contracting HIV among a predominantly heterosexual population; a recent gonorrhea diagnosis was associated with a greater than two-fold increase in HIV seroconversion in men.
High STD rates are also associated with high HIV rates in some populations of men who have sex with men (MSM), and may act as a predictor of an impending rise in HIV incidence. At the 7th Conference on Retroviruses and Opportunistic Infections (CROI) in San Francisco this past winter, L. Torian and colleagues presented study results showing that among MSM in New York City, the presence of syphilis or gonorrhea was a predictor of HIV infection. Because of this close association between HIV and STDs, according to the CDC, "STD surveillance can provide important indications of where HIV infection may spread, and where efforts to promote safer sexual behaviors should be targeted."
Also at the Durban conference, H. Chesson and colleagues from the CDC used a mathematical model to estimate that 5,052 new cases of HIV are attributable to STDs, including chlamydia (3,249 cases), syphilis (1,002 cases), gonorrhea (430 cases), and herpes (371 cases). At the 40th ICAAC held this year in Toronto, N.M. Ferguson and colleagues from Oxford University presented results derived from a mathematical model that suggested that STDs have a greater effect on HIV infectiousness (how likely people are to transmit HIV) than on HIV susceptibility (how likely they are to contract the virus).
STDs Increase Risk for HIV
At the XI International Conference on AIDS held in Vancouver, Canada, in July 1996, Judith Wasserheit, MD, MPH, of the CDC presented a literature review of STDs and HIV transmission. An analysis of multiple studies on four continents showed that persons with both ulcerative and nonulcerative STDs have a 2-5 times greater risk of becoming infected with HIV. The presence of an STD increases both susceptibility to and infectiousness of HIV, a phenomenon Wasserheit referred to as "epidemiological synergy" when she first reported on this connection in 1992. This so-called "STD cofactor effect" for HIV transmission has been demonstrated for syphilis, chancroid, genital herpes, gonorrhea, chlamydia, and trichomoniasis; recent evidence suggests that bacterial vaginosis is also implicated in increased HIV transmission.
Having an STD can make it easier to become infected with HIV due to various biological mechanisms. First, a person who has an STD that causes genital ulcers -- namely syphilis, chancroid, or genital herpes, sometimes referred to collectively as genital ulcer disease (GUD) -- is more likely to contract HIV from an infected person because the open sores can serve as a portal for HIV to enter the body. Second, STDs may increase the risk of contracting HIV by affecting the integrity of cells. At the 12th World AIDS Conference, held in Geneva, Switzerland, in June 1998, researchers from the CDC presented evidence that in people with certain STDs, epithelial cells lining the genital and urinary tracts do not function properly, resulting in gaps between the cells that make it easier for HIV to enter. Third, the presence of an STD increases the concentration of dendritic or Langerhans cells and CD4 T-cells (types of white blood cells) in the genital area and genital fluids, since these cells migrate to the site of an infection. Increased numbers of white blood cells present additional targets for HIV infection. This mechanism applies to nonulcerative STDs -- such as chlamydia, gonorrhea, and trichomoniasis -- as well as ulcerative STDs.
The presence of an STD also makes it more likely that a coinfected person will transmit HIV. First, the virus can be transmitted through open genital lesions, which may come into contact with a partner's vaginal, anal, or oral mucous membranes during sexual activity. HIV is routinely detected in the fluid exuded from most types of genital ulcers in men and women with HIV; and these ulcers also may bleed. D. Cameron and colleagues reported in a 1989 issue of the Lancet that HIV positive women with STD-associated genital ulcers were more likely to transmit HIV to their male partners than HIV positive women without such ulcers. Second, HIV positive people with inflammatory STDs such as chlamydia or gonorrhea are more likely both to shed HIV in their semen and cervicovaginal fluids, and to have greater amounts of HIV in these fluids, compared to HIV positive people without STDs. In the June 28, 1997 issue of the Lancet, Myron Cohen, MD, and colleagues reported that, on average, semen HIV viral load was eight times higher in HIV positive Malawian men with urethritis compared to men without the condition, despite similar blood viral loads. After STD treatment, the men's semen HIV viral loads returned to levels comparable to those of men without STDs. M. Laga presented evidence at the 6th CROI, held in Chicago in 1999, that HIV viral loads were also higher in the cervicovaginal fluids of women with an STD. At this year's CROI, P.F. Barroso, MD, and colleagues from Johns Hopkins University demonstrated that some men whose semen HIV viral load decreased to undetectable levels with antiretroviral therapy experienced an increase in semen viral load after they acquired an STD. Barroso also reported at the 39th ICAAC in 1999 that men with genital warts had a significantly higher HIV viral load in their semen than those without genital warts.
How HIV Impacts Specific STDs
In addition to the epidemiological synergy between STD and HIV transmission, immune damage related to HIV can influence the progression of STDs. Several studies have shown that various STD symptoms may be more severe, last longer, and be harder to treat in people coinfected with HIV. In fact, some sexually transmitted organisms, such as CMV and Candida, may not cause illness at all in persons with intact immune systems, but can cause serious symptoms in persons with HIV/AIDS.
Herpes lesions may be more severe and longer-lasting, and outbreaks may occur more frequently in people with HIV/AIDS. Some people coinfected with HIV and HSV require suppressive oral antiviral therapy to keep outbreaks in check. Herpes is one of the ulcer-producing STDs that can facilitate HIV transmission, since HIV may be shed through the open lesions.
Persons coinfected with HIV and HPV are more likely than HIV negative persons to develop multiple genital warts and warts that endure longer, as well as giant condyloma that can grow rapidly to a large size, potentially obstructing the vagina, anus, or throat and necessitating surgical removal. These more severe warts are less likely to develop in HIV positive people on successful antiretroviral regimens. Even more worrisome, several studies have shown that women with HIV are more likely to develop cervical and anal dysplasia, and sexually active MSM with HIV are more likely to develop anal dysplasia. Most experts recommend more frequent cervical and anal Pap smears for women with HIV, followed by colposcopy if abnormal cells are present; some recommend annual screenings, while others suggest testing every six months. A recent study published by Joel Palefsky, MD, and colleagues from the University of California at San Francisco (UCSF) and the Harvard School of Public Health predicted that regular anal Pap smears could reduce anal cancer in gay men with HIV. According to Dr. Palefsky, "The hope is that a simple, early screening procedure for HPV-induced anal cancer would lead to a . . . drop in disease and death" similar to that seen in women who receive regular cervical Pap smears. The research appeared in the June 1, 2000 issue of the American Journal of Medicine. Recent studies suggest that HPV-related dysplasia may progress more slowly in HIV positive people treated with effective anti-retroviral regimens.
Writing in the August 1998 issue of HIV Newsline, Jeanne Marrazzo, MD, and Christina Marra, MD, noted that coinfection with HIV could complicate the diagnosis and treatment of syphilis. In some cases, syphilis has been known to progress from primary to tertiary stages in just a few years in people with HIV, compared to decades in HIV negative persons. It is unclear whether HIV infection makes it more likely that a person coinfected with Treponema pallidum will develop neurosyphilis, since studies have yielded conflicting results. Likewise, experts are divided about whether cerebrospinal fluid examination for neurosyphilis should be routinely done in HIV positive persons with early-stage syphilis. Treatment is also controversial, with one multicenter trial suggesting that treatment for primary and tertiary syphilis was less likely to be successful in people with HIV. The CDC's 1998 STD treatment guidelines recommend, however, that HIV positive and HIV negative persons with early syphilis should receive the same treatment (single-dose benzathine penicillin); some experts prefer a more aggressive approach (e.g., three weekly injections of benzathine penicillin) for persons with HIV.
Bacterial vaginosis is common in women with HIV. Robert Goldenberg, MD, of the University of Alabama at Birmingham conducted a study showing that coinfected pregnant women were more likely to transmit HIV to their infants, in part due to the increased likelihood of premature rupture of placental membranes and inflammation of the chorionic and amniotic membranes. A study conducted by M. Cohen, MD, presented at the Durban AIDS conference showed that women with HIV were almost twice as likely as women without HIV (78% vs. 39%) to have plasma cell endometritis, an inflammation of the endometrium (lining of the uterus) that is associated with PID.
Many other STDs can be more severe in people with HIV/AIDS. Scabies -- usually a fairly benign, if annoying, condition -- can develop into Norwegian scabies, characterized by crusted, highly contagious and scaly skin lesions. HIV positive women are more likely than HIV negative women to have vulvovaginal candidiasis; in fact, it is often one of the first manifestations of HIV disease in women. Vaginal candidiasis in women with HIV may be severe and recurrent, and may require systemic suppressive antifungal treatment. Molluscum contagiosum outbreaks can be more widespread in people with HIV/AIDS; some people have reported that molluscum lesions resolve with successful antiretroviral treatment for HIV. Various parasitic infections such as Cryptosporidium, Microsporidium, and Isospora are especially harmful in people with suppressed immune systems, to the extent that they are considered OIs.
In addition, because some anti-HIV medications can cause symptoms that mirror those of intestinal parasites (e.g., diarrhea, abdominal cramps), parasitic infections may go unnoticed and untreated.
Some evidence also suggests that STDs may also affect HIV disease progression. J.N. Nkengasong reported at the Durban AIDS conference that among female sex workers with HIV in Abidjan, Côte d'Ivoire, coinfection with gonorrhea was associated with significantly higher HIV plasma viral loads, while coinfection with chlamydia, syphilis, and trichomoniasis were not. CD4 cell counts were also lower in women with STDs (an average of 488 cells/mm3) compared to women without STDs (an average of 640 cells/mm3).
Do STD Programs Influence HIV Rates?
Because of the associations between HIV and STDs, many experts believe that integrated programs to prevent and manage the diseases together are likely to be more effective than programs that treat HIV and STDs as distinct problems.
STD control measures have been in place for decades. When AIDS was first recognized in the U.S. in the early 1980s, many new prevention programs were put in place, followed in the late 1980s and 1990s by service organizations to provide supportive care and treatment, which were not linked to the public health infrastructure dealing with STDs. There were several reasons for this, including the gay community's mobilization to create services for community members afflicted by HIV/AIDS. In addition, people with HIV/AIDS and their advocates were reluctant to accept traditional public health measures, such as contact tracing of sexual partners and names-based reporting, that are widely used to control other STDs. Over the past decade, however, studies have provided evidence that integrated STD and HIV control may be more effective, both globally and in the U.S.
Epidemiological research suggests that community-wide interventions to detect and treat STDs may reduce the incidence of HIV in a population. However, results are conflicting, and the magnitude of this effect is unknown. Notably, the two most well-known studies of STD interventions to prevent HIV transmission in Africa offered opposite results.
The first study took place in the rural Mwanza district of Tanzania. This randomized, controlled trial involved 12,000 adults in 12 matched villages. A comprehensive STD control program was instituted in six of the communities, which included improved STD clinic services, training of health-care providers in STD detection and treatment, ensuring availability of effective antibiotic drugs for curable STDs, and an ongoing STD education and outreach effort. The control villages continued their existing HIV prevention and treatment programs. After two years, the communities with the new STD control programs had a 42% lower incidence of heterosexually transmitted HIV than the control villages. The lower incidence was not related to changes in sexual behavior or condom use in the two sets of villages. Interestingly, the villages with the intervention had only slightly lower STD rates. The STD program cost just over $200 U.S. per HIV infection averted. Results of the Mwanza study were published in the August 26, 1995 issue of the Lancet and presented by Heiner Grosskurth and colleagues at the 1996 AIDS conference.
The second study, known as the Rakai STD Control for AIDS Prevention Study, was conducted in the Rakai district of Uganda. In this study, begun in 1994, researchers randomly assigned 56 villages to either an STD intervention or a control arm. The 6,602 HIV negative adults in the experimental arm received antibiotic treatment at home for a variety of STDs every ten months regardless of whether or not they exhibited STD symptoms. Treatment consisted of single oral doses of azithromycin, ciprofloxacin, and metro-nidazole, plus penicillin injections for those with blood tests that indicated syphilis. The 6,124 adults in the control arm did not receive such treatment. Both HIV and STDs were common in both groups, with STD rates ranging from 50% for bacterial vaginosis to 2% for gonorrhea. The Rakai trial did not include an ongoing program of STD education, diagnosis, or treatment. After the second two-month period, there was no difference in HIV incidence rates in the treatment and control arms; the rate of new HIV infections increased slightly for both groups. However, rates of curable STDs were reduced significantly, and maternal and infant health improved in the treatment arm. Results of the Rakai study were presented by Maria Wawer, MD, and colleagues at the 1998 AIDS Conference and published in the December 12, 1999 issue of the Lancet.
A comparison of the results of the two studies suggests that intensive, continuous, and ongoing STD prevention and control programs -- which could help control STD treatment failures, recurrences, and reinfections -- are likely more effective in reducing HIV than intermittent STD treatment. Also, the Tanzanian communities were at an early stage of the HIV epidemic, with an HIV prevalence rate of about 4%, while the Uganda communities were at a later stage, with an HIV prevalence rate of about 16%, suggesting that STD treatment may have a greater effect in reducing HIV transmission when HIV is less widespread. According to Wawer, "It may be that if you're exposed to a lot of HIV, and the risk is high enough and frequent enough, sooner or later you're going to get it, whether you have an STD or not." Also, persons in the Mwanza study were treated when they had STD symptoms, unlike those in the Rakai trial; treatment of symptomatic persons is likely to have a greater influence in reducing HIV transmission. A comparative presentation of the Mwanza and Rakai trials was published in the June 3, 2000 issue of the Lancet.
It is uncertain whether STD detection and treatment programs will have the same success in the U.S. as they had in Tanzania. The impact may be less because U.S. populations have an overall lower prevalence of STDs and less heterosexual transmission of HIV, and because existing STD control programs are more extensive and accessible than they are in resource-poor countries. However, William Kassler, MD, and colleagues from the CDC reviewed several local and national surveys conducted between 1990 and 1997. At the 1998 AIDS conference they reported that STD rates and HIV incidence in some U.S. populations, especially among young women, approach those found in Africa. The researchers concluded that "while the potential impact of [an STD control program] in the U.S. cannot be precisely quantified until implemented, the rates of STDs among certain groups at high risk for HIV suggest that the impact could be significant," and recommended controlled studies to assess the impact of STD interventions on HIV transmission.
Richard Rothenberg, MD, and colleagues from Emory University estimated that identifying and treating persons coinfected with both HIV and another STD could reduce the risk of HIV transmission to an uninfected sexual partner by 27%; their findings were reported in the August 2000 issue of Sexually Transmitted Diseases. The researchers examined 1-2 years' worth of data on over 4,000 HIV positive persons treated at eight STD clinics in the U.S. during the early and mid-1990s. STD/HIV coinfection rates ranged from 13.9% in Miami to 67.6% in Chicago. The researchers calculated that the risk of HIV transmission from a coinfected person was three times higher than the risk of HIV transmission from an HIV positive person who did not also have another STD. The estimated potential reduction in HIV transmission that could be achieved with STD treatment ranged from 10% at the Los Angeles site to 38% at the Colorado Springs site. The researchers further estimated that if each coinfected person had only one unprotected sexual contact with an HIV negative person, 28 new HIV infections would likely occur from persons with untreated STDs, versus 16 new infections from people whose STDs were treated. According to Rothenberg, "effective treatment of . . . STDs [in coinfected persons] and interventions targeted to their social milieu should be implemented."
STD-HIV Recommendations
Because detecting and treating STDs can be such an effective tool in preventing HIV transmission, the CDC's Advisory Committee on HIV and STD Prevention (ACHSP) suggests that strong linkages should be developed between STD and HIV programs, especially those that target high-risk groups such as heterosexually active young women. The Center for AIDS Prevention Studies (CAPS) at UCSF suggests that in addition to combining STD and HIV control programs, family planning programs should be integrated as well, since measures such as condom use can effectively address all three issues, and because young people are more likely to know someone who has had an STD or an unintended pregnancy than they are to know someone with HIV.
Because people with STDs are so often asymptomatic, the ACHSP recommends that expanded outreach and screening should be done to reach people who are not likely to make use of STD clinic services. Screening for chlamydia, gonorrhea, and syphilis, in particular, should be offered to all sexually active adolescents and young adults. Presumptive treatment, which is started before lab test results confirm a diagnosis, is appropriate for some populations, both because of the likelihood of transmitting an STD while waiting for test results and the unlikelihood of returning to a facility to receive results and treatment. STD detection and treatment services should be available at low or no cost, and should be provided at convenient locations and times, including evenings and weekends. Such services should be made available at hospital walk-in clinics and emergency rooms, community and migrant-worker health centers, family planning clinics, school-based clinics and other clinics for adolescents, correctional facility clinics, primary care physicians' offices, and managed care institutions, as well as dedicated STD clinics.
In addition, STD screening and treatment should be a routine part of the care of persons with HIV. A recommended annual STD screening should include urine tests for chlamydia and gonorrhea, an RPR test for syphilis, a stool test for intestinal parasites, a test for hepatitis virus antibodies, and a vaginal and/or anal Pap smear. Sexually active people should be offered the HBV vaccine.
According to the ACHSP, "Early detection and treatment of curable STDs should become a major, explicit component of comprehensive HIV prevention programs at the national, state, and local levels . . . In areas where STDs that facilitate HIV transmission are prevalent, screening and treatment programs should be expanded."
Liz Highleyman is a freelance medical writer.
CDC National STD Hotline: 800-227-8922
American Social Health Association (ASHA) NIAID Sexually Transmitted Diseases Fact Sheets Barroso, P.F. and others. Predictors of seminal viral load (SVL) suppression in subjects starting antiretroviral therapy (ART). 7th Conference on Retroviruses and Opportunistic Infections. San Francisco. January 30-February 2, 2000. Abstract 471. Centers for Disease Control and Prevention. HIV prevention through early detection and treatment of other sexually transmitted diseases -- United States. Recommendations of the Advisory Committee for HIV and STD Prevention. Morbidity and Mortality Weekly Report 47 (RR-12): 1-24. July 31, 1998. www.cdc.gov/mmwr/preview/mmwrhtml/00054174.htm. Centers for Disease Control and Prevention. 1998 guidelines for treatment of sexually transmitted diseases. Morbidity and Mortality Weekly Report 47 (RR-1): 1-118. January 23, 1998. www.cdc.gov/mmwr/preview/mmwrhtml/00050909.htm. Chesson, H. STDs and the increased risk for HIV transmission: implications for cost-effectivness analyses of STD prevention interventions. XIII International AIDS Conference. Durban, South Africa. July 9-14, 2000. Abstract WePpC1321. Cohen, M.S. and others. Reduction of concentration of HIV-1 in semen after treatment of urethritis: implications for prevention of sexual transmission of HIV-1. Lancet 349: 1868-1873. 1997. Ferguson, N.M. and others. Modeling the role of different sexually transmitted infections on HIV transmission dynamics. 40th Interscience Conference on Antimicrobial Agents and Chemotherapy. Toronto. September 16-20, 2000. Abstract 1198. Grosskurth, H. and others. Control of sexually transmitted diseases for HIV-1 prevention: understanding the implications of the Mwanza and Rakai trials. Lancet 355(9219): 1981. June 3, 2000. Grosskurth, H. and others. Impact of improved treatment of sexually transmitted diseases on HIV infection in rural Tanzania: randomized controlled trial. Lancet 346: 530-536. 1995. Hanson, J. Ulcerative and non-ulcerative STD increase HIV seroincidence in the US: results from a longitudinal study in New Orleans, Louisiana, 1990-1998. XIII International AIDS Conference. Abstract ThOrC725. Institute of Medicine Committee on Prevention and Control of Sexually Transmitted Diseases. The Hidden Epidemic: Confronting Sexually Transmitted Diseases. Eng, T.R. and Butler, W.T., editors. National Academy Press, Washington, DC. 1997. Kassler, W. and others. STD control for HIV prevention in the US: is there likely to be an impact? 12th World AIDS Conference. Geneva, Switzerland. June 28-July 3, 1998. Abstract 525/33238. Laga, M. STD control to prevent HIV: controversies surrounding two recent clinical trials: Mwanza vs. Rakai. 6th Conference on Retroviruses and Opportunistic Infections. Chicago. January 31-February 4, 1999. Abstract S32. Nkengasong, J.N. and others. Impact of sexually transmitted diseases (STDs) on plasma HIV-1 viral load (VL) and immune activation markers among HIV-1 seropositive female sex workers (FSWs) in Abidjan, Côte d'Ivoire. XIII International AIDS Conference. Abstract WeOrB613. Rothenberg RB, and others. The effect of treating sexually transmitted diseases on the transmission of HIV in dually infected persons: a clinic-based estimate. Ad Hoc STD/HIV Transmission Group. Sexually Transmitted Diseases 27: 411-416. 2000. Spruance, S. Gender-specific efficacy of a prophylactic SBAS4-adjuvanted gD2 subunit vaccine against genital herpes disease: results of two clinical efficacy trials. 40th Interscience Conference on Antimicrobial Agents and Chemotherapy. Abstract L-6. Torian, L. and others. High HIV seroprevalence associated with diagnosis of gonorrhea or syphilis in men who have sex with men. 7th Conference on Retroviruses and Opportunistic Infections. Abstract 468. Wasserheit, J.N. Epidemiological synergy: interrelationships between human immunodeficiency virus infection and other sexually transmitted diseases. Sexually Transmitted Diseases 19: 61-77. 1992. Wawer, M.J. and others. Control of sexually transmitted diseases for AIDS prevention in Uganda: a randomized community trial. Lancet 353(9152): 525. February 1999.
ASHA Herpes Hotline: 919-361-8488
Selected Sources
Back to the SFAF BETA Autumn, 2000 contents page.
American Social Health Association (ASHA)
NIAID Sexually Transmitted Diseases Fact Sheets
Barroso, P.F. and others. Predictors of seminal viral load (SVL) suppression in subjects starting antiretroviral therapy (ART). 7th Conference on Retroviruses and Opportunistic Infections. San Francisco. January 30-February 2, 2000. Abstract 471.
Centers for Disease Control and Prevention. HIV prevention through early detection and treatment of other sexually transmitted diseases -- United States. Recommendations of the Advisory Committee for HIV and STD Prevention. Morbidity and Mortality Weekly Report 47 (RR-12): 1-24. July 31, 1998. www.cdc.gov/mmwr/preview/mmwrhtml/00054174.htm.
Centers for Disease Control and Prevention. 1998 guidelines for treatment of sexually transmitted diseases. Morbidity and Mortality Weekly Report 47 (RR-1): 1-118. January 23, 1998. www.cdc.gov/mmwr/preview/mmwrhtml/00050909.htm.
Chesson, H. STDs and the increased risk for HIV transmission: implications for cost-effectivness analyses of STD prevention interventions. XIII International AIDS Conference. Durban, South Africa. July 9-14, 2000. Abstract WePpC1321.
Cohen, M.S. and others. Reduction of concentration of HIV-1 in semen after treatment of urethritis: implications for prevention of sexual transmission of HIV-1. Lancet 349: 1868-1873. 1997.
Ferguson, N.M. and others. Modeling the role of different sexually transmitted infections on HIV transmission dynamics. 40th Interscience Conference on Antimicrobial Agents and Chemotherapy. Toronto. September 16-20, 2000. Abstract 1198.
Grosskurth, H. and others. Control of sexually transmitted diseases for HIV-1 prevention: understanding the implications of the Mwanza and Rakai trials. Lancet 355(9219): 1981. June 3, 2000.
Grosskurth, H. and others. Impact of improved treatment of sexually transmitted diseases on HIV infection in rural Tanzania: randomized controlled trial. Lancet 346: 530-536. 1995.
Hanson, J. Ulcerative and non-ulcerative STD increase HIV seroincidence in the US: results from a longitudinal study in New Orleans, Louisiana, 1990-1998. XIII International AIDS Conference. Abstract ThOrC725.
Institute of Medicine Committee on Prevention and Control of Sexually Transmitted Diseases. The Hidden Epidemic: Confronting Sexually Transmitted Diseases. Eng, T.R. and Butler, W.T., editors. National Academy Press, Washington, DC. 1997.
Kassler, W. and others. STD control for HIV prevention in the US: is there likely to be an impact? 12th World AIDS Conference. Geneva, Switzerland. June 28-July 3, 1998. Abstract 525/33238.
Laga, M. STD control to prevent HIV: controversies surrounding two recent clinical trials: Mwanza vs. Rakai. 6th Conference on Retroviruses and Opportunistic Infections. Chicago. January 31-February 4, 1999. Abstract S32.
Nkengasong, J.N. and others. Impact of sexually transmitted diseases (STDs) on plasma HIV-1 viral load (VL) and immune activation markers among HIV-1 seropositive female sex workers (FSWs) in Abidjan, Côte d'Ivoire. XIII International AIDS Conference. Abstract WeOrB613.
Rothenberg RB, and others. The effect of treating sexually transmitted diseases on the transmission of HIV in dually infected persons: a clinic-based estimate. Ad Hoc STD/HIV Transmission Group. Sexually Transmitted Diseases 27: 411-416. 2000.
Spruance, S. Gender-specific efficacy of a prophylactic SBAS4-adjuvanted gD2 subunit vaccine against genital herpes disease: results of two clinical efficacy trials. 40th Interscience Conference on Antimicrobial Agents and Chemotherapy. Abstract L-6.
Torian, L. and others. High HIV seroprevalence associated with diagnosis of gonorrhea or syphilis in men who have sex with men. 7th Conference on Retroviruses and Opportunistic Infections. Abstract 468.
Wasserheit, J.N. Epidemiological synergy: interrelationships between human immunodeficiency virus infection and other sexually transmitted diseases. Sexually Transmitted Diseases 19: 61-77. 1992.
Wawer, M.J. and others. Control of sexually transmitted diseases for AIDS prevention in Uganda: a randomized community trial. Lancet 353(9152): 525. February 1999.


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There have been several stories in the news lately about hundreds of Harry Potter fans becoming "bored†with the pet owls that the popular movie series inspired their parents to purchase as pets for them.
Really? Purchasing an owl for your child because it looked cute in a movie? I have to wonder what thought process is involved with the purchase of an owl as a pet. What did parents think would happen?
Unfortunately, instead of the owls coming with a wand that you wave at them after purchase rendering them "magical†and providing a super cool and efficient system for supernatural mail delivery (and who wouldn't want a nocturnal animal that poops pellets of rat bones), owls are expensive, extremely high maintenance (duh), require a lot of care and responsibility and can live for decades.
To top it off, most have at least a five-foot wing span and need to flap their wings continuously to avoid chest infections.
So, naughty pet-parents are illegally releasing the previously captive pet owls into the wild, where the owls are starving to death or proceeding to kill other smaller owls, thus causing mayhem in the natural order of the universe. Unfortunately this happens with many wild animals that are not good candidates for pets, with tragic results.
Case-in-point: How many people do you know that have purchased cute little bunnies for their children as Easter gifts?
Remember the Teenage Mutant Ninja Turtle film in the 1990s? That movie inspired a craze of pet turtles that ended up dumped in rivers, canals and lakes. Why? Because they apparently weren't as cool, mutant and ninja as they were in the movie AND they posed a huge risk for salmonella poisoning in children!
A Japanese cartoon called "Rascal the Raccoon†aired in 1977 about an American boy befriending a raccoon. The outcome? The entire raccoon population of Japan, that's what. The Japan Times reported in 2004: "Owners, fed up with trying to tame the wild species to be cute little critters like the one in the cartoon, dumped them in the wild – where, lacking a natural predator – they have proliferated and are now perceived as pests, occasionally damaging crops and bothering people.â€
Will we never learn? Do not adopt a "pet†because it's cute or you saw it in a movie, etc. Pet-flings almost always go wrong and always end BADLY for the animal.

subset: commoncrawl


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Hope Summer Repertory Theatre's Children's Performance Troupe began its season June 18 with " Sarah Plain and Tall" by Joseph Robinette, based on the Newbery Award-winning book by Patricia MacLachlan.
Hope Summer Repertory Theatre's Children's Performance Troupe began its season June 18 with " Sarah Plain and Tall" by Joseph Robinette, based on the Newbery Award-winning book by Patricia MacLachlan.
This will be followed by CPT's second show, "Petite Rouge, the Cajun Red Riding Hood," with music and lyrics by author Joan Cushing, also writer of HSRT's past favorite "Miss Nelson is Missing" and "Junie B. Jones," beginning July 16. Both performances are held in the DeWitt Studio Theatre.
"Sarah Plain and Tall," directed by Diana Robbins, tells the story of a willful woman who answers the newspaper ad of a widower, and moves to the Midwest to help him raise his children. Despite initial hardships, Sarah wins the whole family over with her love, laughter, and cheer.
James Saba directs the hilariously spicy musical "Petite Rouge, the Cajun Red Riding Hood." Petite Rouge is a duckling who leads a giant gator on a wild chase through the New Orleans swamp with the help of his cat friend Tejean.
Tickets have already gone on sale at both the DeVos Fieldhouse and the DeWitt Theatre Ticket Office and are going fast! All tickets are $10 for general admission.
The ticket office is open from 10 a.m. to 5 p.m. Monday through Friday. Beginning June 14 the ticket office is open on Saturday's at noon. On performance dates, the DeWitt Ticket Office will be open through intermission. The ticket office is located in the DeWitt Cultural Center at 12th Street and Columbia Avenue. For tickets call the ticket office at 616-395-7890.
For more information visit the HSRT website at www.hope.edu/hsrt
The DeWitt Theatre is located at 141 East 12th Street. While 12th Street is under construction, the DeWitt and Martha Miller parking lots are both accessible from the North.
And while at the ticket office, make sure to check out HSRT's other productions
such as "Kiss Me Kate," "Forever Plaid," the cabaret at Till Midnight, "Closer Than Ever" opening July 5, "The Foreigner" opening July 11, and "Doubt, A Parable" opening July 18.


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Abstract and Keywords
Chaos theory and complexity theory, collectively known as nonlinear dynamics or dynamical systems theory, provide a mathematical framework for thinking about change over time. Chaos theory seeks an understanding of simple systems that may change in a sudden, unexpected, or irregular way. Complexity theory focuses on complex systems involving numerous interacting parts, which often give rise to unexpected order. The framework that encompasses both theories is one of nonlinear interactions between variables that give rise to outcomes that are not easily predictable. This entry provides a nonmathematical introduction, discussion of current research, and references for further reading.
Keywords: agent-based models, chaos theory, complexity theory, dynamical systems, nonlinear dynamics, system dynamics
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text: Maria explaining the play to a Christian Group Maria explains the play to a Christian group. The bald guy on her right is the priest. Apparently this whole group likes to take in theatre together. Share this:TwitterFacebookMoreEmailPrintPocketLike this:Like Loading... Related Author: Blaine L. Reininger Blaine L. Reininger was born July 10, 1953 in Pueblo, Colorado. Then he lived a life. By and by, he founded Tuxedomoon with Steven Brown in 1977. He traipsed around America, tuxedomooning until 1980, when he began to traipse around Europe. As a direct result of all of this traipsing, many musical compositions were composed, most of which found their way to some sort of mechanical device capable of reproducing musical compositions. This was mostly for the good. He now lives in Athens, Greece, where he is content. View all posts by Blaine L. Reininger


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Baradin Hold
- Argaloth – Unable to contain the massive pit lord Argaloth in the cells of Dalaran's mighty Violet Hold, the magi of the Kirin Tor were left with no choice but to confine the powerful demon beneath Tol Barad.
- Occu'thar – This ravenous demon broke free of its cage and gained access to the western wing of the prison, devouring all of the inmates held there. Occu'thar's gluttony resulted in a body too bloated to escape its environs, effectively turning the prison wing into its new holding cell.
- Alizabal, Mistress of Hate – The Kirin Tor imprisoned Alizabal in their formidable Violet Hold not long after corrupt magi summoned the shivarra into Azeroth. Despite arcane wards restricting her powers, the demon's malicious influence alone caused her guards to murder one another in sudden fits of rage. Her transfer to Baradin Hold prior to the Cataclysm has only aggravated the ruined prison's increasingly dire conditions.
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The Wowhead Client is a little application we use to keep our database up to date, and to provide you with some nifty extra functionality on the website!
It serves 2 main purposes:
- It maintains a WoW addon called the Wowhead Looter, which collects data as you play the game!
- It uploads the collected data to Wowhead in order to keep the database up-to-date!
You can also use it to keep track of your completed quests, recipes, mounts, companion pets, and titles!
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For many who survey an African landscape strewn with political wreckage, nowadays merely to raise the subject of European colonialism, which formally ended across most of the continent five decades ago, is to ring alarm bells of excuse making.
Clearly, the African disaster most in view today is Sudan, or more specifically the dirty war that has raged since 2003 in that country's western region, Darfur.
Rare among African conflicts, it exerts a strong claim on our conscience. By instructive contrast, more than five million people have died as a result of war in Congo since 1998, the rough equivalent at its height of a 2004 Asian tsunami striking every six months, without stirring our diplomats to urgency or generating much civic response.
Mahmood Mamdani, a Ugandan-born scholar at Columbia University and the author of "When Victims Become Killers: Colonialism, Nativism, and Genocide in Rwanda," is one of the most penetrating analysts of African affairs.
In "Saviors and Survivors: Darfur, Politics, and the War on Terror," he has written a learned book that reintroduces history into the discussion of the Darfur crisis and questions the logic and even the good faith of those who seek to place it at the pinnacle of Africa's recent troubles. It is a brief, he writes, "against those who substitute moral certainty for knowledge, and who feel virtuous even when acting on the basis of total ignorance."
Mr. Mamdani does not dismiss a record of atrocities in Darfur, where 300,000 have been killed and 2.5 million been made refugees, yet he opposes the label of genocide as a subjective judgment wielded for political reasons against a Sudanese government that is out of favor because of its history of Islamism and its suspected involvement in terror.
At his most provocative Mr. Mamdani questions the distinction between what is often labeled counterinsurgency and genocide, saying the former, even when it kills more people, is deemed "normal violence" while the latter is considered "amoral, evil," and typically it is the West that does the labeling.
Although he uses the United States war in Iraq as an example, with the International Criminal Court recently issuing an arrest warrant for Sudan's leader, Omar Hassan al-Bashir, Mr. Mamdani's most compelling example is the treatment of a crisis in neighboring Uganda.
In Uganda, long one of Washington's closest African friends, Mr. Mamdani traces the history of ethnically targeted "civilian massacres and other atrocities" against the brutal insurgency known as the Lord's Resistance Army.
In 1996, under President Yoweri Museveni, a second phase of that war began "with a new policy designed to intern practically the entire rural population of the three Acholi districts in northern Uganda," Mr. Mamdani writes.
"It took a government-directed campaign of murder, intimidation, bombing and burning of whole villages to drive the rural population into I.D.P. (internally displaced persons) camps."
In 2005 Olara Otunnu, a former Ugandan ambassador to the United Nations, denounced the government's tactics, saying, "An entire society is being systematically destroyed — physically, culturally, socially and economically — in full view of the international community."
But as elsewhere in Africa, Mr. Mamdani says, the International Criminal Court has brought a case against only the enemy of Washington's friend, the Lord's Resistance Army, remaining mute about large-scale atrocities that may have been committed by the Ugandan government.
In this pattern the author sees the hand of politics more than any real attachment to justice. Many argue that what makes Darfur different from other African crises is race, with the conflict there pitting Arabs against people often called "black Africans," but here again Mr. Mamdani takes on conventional wisdom.
"At no point," he states flatly, "has this been a war between 'Africans' and 'Arabs.' "
Much foreign commentary about Sudan speaks of its Arabs as settlers, with the inference that they are somehow less African than people assumed to be of pure black stock.
If whites in Kenya and Zimbabwe, not to mention South Africa, vociferously maintain their African-ness, what then to make of the Arab presence in Sudan, whose slow penetration and widespread intermarriage, Mr. Mamdani writes, "commenced in the early decades of Islam" and "reached a climax" from the 8th to the 15th century, "when the Arab tribes overran much of the country"?
More interestingly, the author maintains that much of what we see today as a racial divide in Sudan has its roots in colonial history, when Britain "broke up native society into different ethnicities, and 'tribalized' each ethnicity by bringing it under the absolute authority of one or more British-sanctioned 'native authorities,' " balancing "the whole by playing one off against the others."
Mr. Mamdani calls this British tactic of administratively reinforcing distinctions among colonial subjects "re-identify and rule" and says that it was copied by European powers across the continent, with deadly consequences — as in Rwanda, where Belgium's intervention hardened distinctions between Hutu and Tutsi.
In Sudan the result was to create a durable sense of land rights rooted in tribal identity that favored the sedentary at the expense of the nomad, or, in the crude shorthand of today, African and Arab.
Other roots of the Darfur crisis lie in catastrophic desertification in the Sahel region, where the cold war left the area awash in cheap weapons at the very moment that pastoralists could no longer survive in their traditional homelands, obliging many to push southward into areas controlled by sedentary farmers.
He also blames regional strife, the violent legacy of proxy warfare by France, Libya and the United States and, most recently, the global extension of the war on terror.
This important book reveals much on all of these themes, yet still may be judged by some as not saying enough about recent violence in Darfur.
Mr. Mamdani's constant refrain is that the virtuous indignation he thinks he detects in those who shout loudest about Darfur is no substitute for greater understanding, without which outsiders have little hope of achieving real good in Africa's shattered lands.
Source: New York Times


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Congress slipped into "stall" mode on all things budgetary this week as talks over how to rein in deficits broke down on key fronts.
Senate Democrats had expected to take up their own budget in committee next week, but instead deferred the markup indefinitely. Senate Budget chair Kent Conrad (D) of North Dakota said that he saw no point in going forward with a partisan budget.
At the same time, Sen. Tom Coburn (R) of Oklahoma, bowed out of the bipartisan Gang-of-Six talks, citing an impasse over entitlement cuts. The talks between the remaining five senators continued, but Coburn's role is seen as critical to sell the plan to conservatives.
National debt ceiling 101: Is a crisis looming?
"They just don't have any desire to compromise," says Stanley Collender, a budget expert and managing director of Qorvis Communications in Washington, commenting on Senate budget negotiations. "If anything, they're further apart."
That leaves bipartisan leadership talks, chaired by Vice President Biden, as the main venue for a deal that could pass both the House and Senate. On Thursday, Senator Conrad in effect deferred to those talks with a view to using the Budget Committee to shepherd a bipartisan leadership deal through the Senate.
"Democrats on the Budget Committee are very close to an agreement. We will have a budget," said Senator Conrad, in a statement. "But after broad consultation, we have decided to defer a budget mark-up because of the high-level bipartisan leadership negotiations that are currently underway."
Aides close to the budget negotiations say that the budget panel was closing in on a deal to cut $4 trillion in spending over 10 years to be achieved by 50 percent spending cuts and 50 percent revenue increases. But Republicans unanimously opposed tax increases, and there were divisions in Democratic ranks that blocked a final agreement.
Sen. Bernard Sanders (I) of Vermont, a member of the Budget panel, was holding out for a 5.4 percent surtax on incomes over 1 million a year, but two Democrats on the panel balked at raising taxes in an economic downturn. Senator Sanders says he will not vote for any budget plan without "shared sacrifice," including tax increases. With the panel nearly evenly divided with 12 Democrats and 11 Republicans (Sen. Sanders aligns himself with the Democrats), his dissent is a critical block to any partisan plan.
"Conrad doesn't see how having a partisan markup now in any way advances the ball," said a Senate Democratic aide. "He is also fearful that a partisan markup would only harden positions."
But Senate Republicans say that the majority is ducking a tough political problem to avoid a backlash from voters over unpopular spending cuts or tax increases. Twenty-three Democrats are up for reelection in 2012, compared with 11 Republicans in the Senate.
"It seems Senate Democrats are desperately trying to avoid having to present a budget to the American people," said Sen. Jeff Sessions (R) of Alabama, the top Republican on the budget panel, in a statement.
"Senator Reid may wish to shield his members from tough votes that expose their unwillingness to cut spending or their eagerness to raise taxes. But that strategy will not hold. The public will be mobilized. Sooner or later every senator will have to stand and be counted," he added.
That leaves the GOP House-passed budget, which cuts $5.8 trillion over 10 years, without raising taxes, as the only budget document currently on the table. The GOP plan, drafted by Rep. Paul Ryan (R) of Wisconsin, converts Medicare to a voucher-based system and passed without a single Democratic vote.
Senate majority leader Harry Reid (D) of Nevada says that the Senate will vote on the GOP House budget next week. On Friday, Senate Democrats released a report predicting a "devastating" fallout, state by state, should that budget be adopted for 2012 spending.
These include the loss of 2 million private sector jobs over the next five, due to proposed cuts to Medicaid, and the doubling of health costs for seniors, due to changes in Medicare.
"Nationwide, nearly 4 million seniors would pay $2.2 billion more for prescription drugs in 2012 alone under the Republican plan," the report concludes.


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Henkel Labeling Adhesives are Casein-Free
- Published: March 05, 2012
DUSSELDORF, GERMANY | Optal XP casein-free labeling adhesives from Henkel offer extended properties and a performance profile said to ensure trouble-free production processes for beverage manufacturers while extending their options.
Company says casein-free adhesives offer a longer shelf life and temperature stability, feature exceptionally good initial tack, and support fast setting and drying, thus helping to reduce adhesive usage rates. Adhesives exhibit good adhesion even to chilled glass surfaces, company adds.
These adhesives, based on synthetic polymers, reportedly contribute to environmentally compatible production by yielding economic and ecological process benefits in terms of mileage and field-proven wash-off behavior. Long-term use by various national and international beverage bottlers has shown that the labels can be detached with ease in bottle washing plants using standard cleaners and settings. In addition, these second-generation adhesives give no cause for concern during waste water treatment, have FDA approval, are free of toxic ingredients, and contain no alkylphenol ethoxylates, zinc, or borax.


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Believe me, I have plenty of reasons to justify using my bike downtown regardless if I ride it all the way or throw it on the front of a bus. It's not like I need any convincing.
Today, while sipping on my daily dose of fatty, caffeinated carbohydrates, I saw a car. I see plenty of them, but this one was pulling in and out of a parallel parking spot. I watched the driver take about nine tries to get her car parallel parked. Three of those attempts resulted in rear-ending a lamp post. Two of them resulted in rolling her rear tire into the curb, another try got her successfully backed ONTO the curb. I believe she probably scraped her front fender on the chrome bumper of a parked pickup truck at least one of the times, and she finally got parked. Not surprising, she was on the cell phone the entire time.
I told JR he could get rich quick if he just stood there on Main street and offered to parallel park these idiots' cars for a few bucks. This and several other snide remarks from me resulted in Lorin and JR calling me a jaded grouch that's crotchety beyond my years. I can't say I disagree with them too much. I could probably blog a few times per week posing as a curmudgeon who's got a serious bone to pick with the world. How'd Lorin word it? Something like "Observations from the rocking chair."
No sooner did the Inner City Soccer Mom (JR's Words, not mine!) finish banging her Grand Prix up on Kansas City's streetscape, a pair of nincompoops in a PT Loser start having the same problem. Four attempts and two scraped wheels later, the driver (if you can call him that) has somehow managed to park, but leaving almost a foot of room between the car and the curb. Look, pal. You already trashed your wheels. There's no need to park in the middle of the traffic lane. He made up for it by backing firmly -- and almost intentionally if I do say so myself -- into the SUV behind him when leaving.
There are other horror stories of people getting their cars damaged in the very same parking garage my bike resides in while I'm at work, too. It's pseudo-valet parking that's 3-4 cars deep. You park, then hand your keys over so the cars can be moved if someone who's boxed in needs to leave. Hard telling if it's other car owners or the "Skilled" valet drivers to blame for dings and dents in the garage. I'm just glad I park on a bike rack by the Motorcycles, where there's plenty of room. Although, now that I watched a Grand Prix successfully back over a 6" curb and into a lamp post, I'm really thinking twice about using lamp posts as improvised bike parking. In fact, I'm wondering if the bike racks that are a full 8' from the street are vulnerable to these drivers.
Random Tunage:
Masters & Nickson - Out there (5th Dimension)
Crystal Method - Blowout
Wednesday, April 02, 2008
Another reason I choose my bike: Bumper Cars!
Believe me, I have plenty of reasons to justify using my bike downtown regardless if I ride it all the way or throw it on the front of a bus. It's not like I need any convincing.
4 comments:
I hear ya. "Observations from the rocking chair" -- great!
- April 03, 2008 9:45 AM
- gwadzilla said...
it really is not that hard to park a car
the driver's test should be more difficult
better yet
they should issue an IQ test to drive
that would put less drivers on teh road
- April 03, 2008 2:54 PM
- Yokota Fritz said...
I'm seeing more than the usual number of folks who can't parallel park.
I learned very recently that California driver test no longer has a parallel parking test! I was in the car with an Indian cow-orker going to lunch. I said, "There's a parking spot! .... there's another! ...
{pause as he continues driving}
Me: "Umm, why are you passing all of these spots?"
Him: "I am sorry. I do not now how to park like that."
Me: "??? Didn't you need to take a driving test when you got your license? What about the parallel parking test?"
Him: "There is no such test."
Me: "!!!"
We did a Chinese fire drill at a stop sign so I could park his car (a little Honda Accord) for him. I learned to drive in Tokyo Japan. Just give me three our four inches of space in front of and behind the car and I'll scoot it in for you. I'm not quite as good as this guy, though.
- April 04, 2008 6:28 PM
- Yokota Fritz said...
- April 04, 2008 6:29 PM
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Hubcap hamburger in Arkansas
by Gary Torres
My too kind and loving wife and I are on vacation headed out to Nashville. I have stopped in Scott, AR, a town so small Monticello would seem like a sprawling metropolis in comparison.
First, I have to tell you that there is a Monticello connection; Eddie Boyle grew up in the area. Eddie has been gone now for 23 years, but he still has some impact in Monticello. I'm seeking insight.
I am going there in hunt of the award-winning "hubcap hamburger", allegedly the best burger in America; even President Clinton frequented this out of the way place.
When I say out of the way, it is only 10 miles off of I-40, but clearly the town is 70 years back in time. When we drive by Cotham's Mercantile, the award winning 101 year old Checker Auto Parts turned restaurant, a couple of hill-billies chewing on a piece of grass watch us as carefully as I might watch a snake crawl over my shoes. I am tempted to break out my guitar, which I brought with me, just to see if someone wants to play Dueling Banjos.
This could be a movie set for the 1972 movie Deliverance; I am sure that I can hear banjos twanging. The hair on my neck stands alert.
We drive slowly past the dilapidated old hardware store, and I assure my too kind and loving wife that can't possibly be the place we are looking for. There is a goat pen with an assortment of other farm critters on the east side of the store, and it looks like a strong wind will blow the building over.
We go into the restaurant, which looks like a dusty-cobwebby Motor Parts with a few tables on one side and an assortment of hoses, fan belts, and other 1960ish automobile parts hanging on peg board.
As we go in and sit down, Daisy-Lou comes by to take our order of fried green tomatoes and the hubcap hamburger. Her t-shirt says, "Where the elite meet to eat."
I expect to see President Clinton and Senator Dave Pryor walk through the door any second or perhaps for one of the banjo-boys to lock the door from the inside and turn with a demonic grin and ask us, "Where you goin' city boy?"
We eat our food with the enthusiasm of a teenage boy after football practice. I can't describe how good the food was, but if I ever go back that way, and I am not saying that I will, I think I would venture another brush with the dueling-banjo-boys to get one more chance to partake of the tastiest burger this cowboy has ever eaten.
The sheriff watches as we drive out of town; we don't look back. No matter. My belly is full, and I am happy to have made it out of the back woods of Arkansas. I can almost hear Eddie in his smooth southern twang say, "You'all come back soon, ya hear!"
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Have mold in your home or office? We are here to tell you how to get rid of that mold yourself or how to get a professional to do it for you! Mold is not only unattractive to have… Read More
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Mold Solutions: How to Get Rid of Mold
- September 2nd, 2011
- Posted in Health Risks
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Google I/O will be starting tomorrow and 5500 developers will come together at the highly anticipated developer conference held by Google. Google's I/O event will also grab more eyeballs after the recent introduction of iOS 6 and Microsoft's Surface tablet and next generation of Windows Phone O.S.
Google will most likely be introducing the latest Android OS; Jelly Bean (see Jelly Bean structure at Googleplex) to the world along with the rumored 7 inch Google Nexus tablet. However, there may be several more announcements which could turn out to be exciting.
Google I/O keynotes are usually streamed online and on YouTube. The first Google I/O keynote will begin on June 27 at 9:30 Am and can be watched at https://developers.google.com/events/io/ or http://www.youtube.com/GoogleDevelopers. You can also find other keynotes and developer events at their I/O live page at https://developers.google.com/events/io/io-live
We will try and add links to videos to these post when the event goes live.